My name's Sheila Donnelly, and I'm from the School of Life Sciences, where we do a lot
of biological research.
For the purpose of today, given I've only got five minutes, I'm going to crush about
ten years of science on a very project that I work on, into hopefully five minutes.
I was going to start with quite a sneaky request for a standing ovation, and I would create
this by asking everyone in the room to stand up if they could answer yes to the following
question: do you know or do you yourself suffer from diabetes, multiple sclerosis, inflammatory
bowel disease, rheumatoid arthritis, cirrhosis and so on.
If anyone in this room knows of someone or themselves suffer from these diseases, you
have an immune-mediated disease, and there's quite a few of us in the country.
This is a disease where your immune response, which has evolved to protect you from infection
from bacteria and viruses, is now turning on your own body.
So for example, type 1 diabetes - the immune response destroys the insulin-producing islet
cells.
In MS, the immune response is destroying the insulation around the nerve cells which is
necessary for communication.
We recognise it's probably an endemic of these immune-mediated diseases.
There's millions of people around the world afflicted by them, and we need to know why.
We don't have a cure for these diseases, nor do we really have an effective treatment.
But we need to understand why these occur in order to develop an effective treatment
- and this is where my work comes in.
Typically people consider these diseases as having a genetic basis, but the rate at which
they're occurring and increasing over time is too fast for these diseases for these to
be genetically based, or certainly solely genetically based.
Instead, we think there's an environmental factor involved.
So either something has come into the environment in the developed world, where these diseases
are found, or an environmental factor is removed.
I will say that this is now where I'm a bit biased.
I'm a parasitologist, but I believe that the environmental factor that's been removed is
parasitic worms.
If you look at these maps on the right-hand-side, we have the instance of diabetes, type one,
and on the left-hand-side, a map where parasitic worms are found endemically - that is, permanently
found within populations in society.
And there's a really nice clear inverse relationship.
So the question is - by removing parasitic worms, are we making ourselves susceptible
to disease?
And how could this possibly be the case?
These worms are pathogens, infectious organisms.
Yes, they are, but they've been around for a very long time.
So we evolved in the presence of these parasitic worms, our immune response was educated in
the presence of these parasitic worms.
So what if I was to tell you that these parasitic worms are in fact part of the immune system?
Perhaps by removing them, we're dis-regulating or unbalancing the immune system.
By taking them out, we're getting auto-immune disease.
If we put them back in, do we balance the immune response?
It may sound crazy, but this gastroenterologist, Joel Weinstock on the right-hand-side, tried
it.
He thought the epidemiological evidence was so compelling that there was definitely truth
to this possibility.
He took 29 patients that had ulcerative colitis, infected them with the pig whipworm, and he
found that most of them went into remission, and remained in remissions four to six years
later.
The caveat?
It was a very small clinical trial, and not blinded, no placebos and so on.
But the data...everybody went crazy, this is fantastic, the first proof of concept that
worms may actually provide therapeutic relief from disease.
So we now have a number of human trials currently ongoing around the world for MS and cirrhosis
and some for asthma, in fact.
We're awaiting the outcomes of those to see how much truth there is to this hypothesis.
So there's evidence that it's good, and it's certainly very encouraging, but there's a
downside, and these pictures on the left will show you.
So the parasitic worms, they need a mammalian host.
If we want to use this as a therapeutic, we need to grow them in a mammalian host, and
collect them in one way.
You can see the picture of the pig, where the arrow's pointing, and you can see the
picture of the human host, where the arrow's pointing.
We collect these from faeces.
So obviously there's a risk, it's not really going to be a global therapeutic.
And again, they are pathogens, so there is physiological outcomes to having a parasitic
worm, so not an ideal solution.
So instead, at UTS, we're taking a different approach, and this slide summarises my entire
life work.
On the right-hand-side, we have the parasitic worm that I work with, and you can see this
beautiful branch structure throughout its body, and that's the gut, its stomach.
It's filled with haemoglobin and lots of other molecules, which the parasite secretes in
order for it to migrate around the host, to feed, to produce eggs and so on.
So we extract the contents of those gut in flasks in the lab, and if we move along, you
can see all my years in one picture.
We can isolate what that worm secretes, identify them, work out what they are, then synthesise
them in the lab as individual molecules, and then use animal models of disease to see if
those individual molecules can provide therapeutic effect.
And I've summarised our most recent and very exciting data on the left side, where we have
a mouse model of multiple sclerosis.
And the black line, which goes in waves, is the control mice, and the flat green line
are those mice that were treated with a single parasite peptide only three times.
So it's very encouraging, we're currently trying to commercialise, so very interesting
to look at our rail at UTS to see where we can progress.
And I would finally just like to acknowledge, as a science project, it has gone on for a
long time with a lot of students and researchers involved.
So thank you, and thank you for your time.